Download Nosocomial Respiratory Syncytial Virus Infections: The “Cold War

590
SPECIAL SECTION: HEALTHCARE EPIDEMIOLOGY
Robert A. Weinstein, Section Editor
Nosocomial Respiratory Syncytial Virus Infections: The “Cold War”
Has Not Ended
Caroline Breese Hall
Departments of Pediatrics and Medicine, University of Rochester
School of Medicine and Dentistry, Rochester, New York
Respiratory syncytial virus (RSV) is a major nosocomial hazard on pediatric wards during
its annual outbreaks. It produces significant morbidity in young children and is most severe
in those with underlying conditions, especially cardiopulmonary and immunosuppressive diseases. In older patients, RSV may exacerbate an underlying condition or pulmonary and
cardiac manifestations. On transplant units, of RSV may be occult and is associated with
high mortality rates. The manifestations of nosocomial RSV infections may be atypical, especially in neonates and immunosuppressed patients, resulting in delayed or missed diagnosis
and adding appreciably to the costs of hospitalization. RSV is primarily spread by close contact
with infectious secretions, either by large-particle aerosols or by fomites and subsequent selfinoculation, and medical staff are often instrumental in its transmission. Thus, integral to any
infection control program is the education of personnel about the modes of transmission, the
manifestations, and the importance of RSV nosocomial infections. Hand washing is probably
the most important infection control procedure. The choice of barrier controls should be
decided by individual institutions depending on the patients, the type of ward, and the benefit
relative to cost.
In days of old the scourge of colds was thought a wen
Of evil humors wrought on hands by sins of men.
A curse for acts we should have done they still may be,
But more, they teach both lords and serfs all risk this fee.
The morbidity engendered by respiratory syncytial virus
(RSV) infections has been recognized now for decades but not
necessarily appreciated. Perhaps the first published description
of nosocomial RSV infections was that of Adams [1], who in
1937 identified outbreaks of pneumonia in the nurseries of 2
Minneapolis hospitals. Thirty-two infants, mostly aged 4–12
weeks, developed pneumonia, and 28% died. All of the infants
who died had cytoplasmic inclusions in the bronchial epithelium. These findings and the distinctive epidemiology and clinReceived 1 May 2000; revised 22 May 2000; electronically published 14
September 2000.
Financial support: This study was supported by grants from the National
Institutes of Health (AI-45248 and RR-00044).
Publication of the Special Section on Healthcare Epidemiology has been
made possible by an educational grant from Pfizer Pharmaceuticals Group,
Pfizer, Inc.
Reprints or correspondence: Dr. Caroline Breese Hall, University of Rochester Medical Center, 601 Elmwood Ave., Box 689, Rochester, NY 14642
([email protected]).
Clinical Infectious Diseases 2000; 31:590–6
q 2000 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2000/3102-0033$03.00
ical presentation of the outbreaks led Adams to suggest that
they were caused by a virus. Two decades later, Adams et al.
[2] studied a markedly similar outbreak of illness in infants and
were able to identify it as being caused by the newly discovered
RSV. Comparing this to the carefully documented clinical and
pathological findings in the earlier nursery outbreaks led Adams to propose that the agent of both was the “chimps coryza
agent,” later rechristened RSV.
Epidemiological and Clinical Characteristics
of Nosocomial RSV Infection
Impact of Nosocomial RSV Infections
In the decades since the study of Adams et al. [2], RSV has
been shown during its yearly appearance to be a major nosocomial hazard for patients of all ages. On pediatric wards, RSV
has been the most frequent cause of nosocomial infection [3–5].
The resulting morbidity and costs have been striking, especially
in infants. About 40% of nosocomial RSV infections are associated with lower respiratory tract disease in this young age
group. Risk factors for acquiring RSV infection while hospitalized during the often-prolonged RSV season, in addition to
young age, also include underlying or chronic disease, long
hospitalization, and crowded, busy wards. Increases in the duration and costs of hospitalization have been significantly correlated with the nosocomial acquisition of RSV infection.
CID 2000;31 (August)
Nosocomial RSV Infections
Clinical Findings in Populations at Risk
Neonates. Nosocomial outbreaks of RSV in neonatal intensive care units, as illustrated by those described by Adams
[1], may be particularly severe, with unexpected clinical manifestations and a high mortality [6–8]. The potential severity
may be aggravated in neonatal units by the difficulty of recognizing an outbreak from an infectious agent or RSV specifically. In neonates, RSV infection is frequently atypical in its
presentation, manifest as nonspecific, nonrespiratory signs that
premature infants develop characteristically from multiple
causes, such as apnea, bradycardia, and changes in feeding and
ventilation.
Medical personnel. RSV infections in medical staff, both
community-acquired and nosocomially acquired, also frequently are not recognized, because they may be mild or manifest as “colds” or flu-like illnesses. More than 50% of staff on
pediatric wards have been shown to become infected with RSV
during periods when RSV is prevalent in the community. Acquisition of RSV infections by medical personnel is of particular
concern. Because the infection lacks distinctive signs and initially sometimes lacks severity, its importance may not be recognized, and staff may become effective but occult vectors for
transmission on the ward. Furthermore, RSV infection may
result in ∼40% of those infected being absent from work during
one of the busiest seasons on hospital wards [9]. Although the
great majority of RSV infections in staff are symptomatic,
asymptomatic infection accompanied by appreciable shedding
of RSV in respiratory secretions occurs in 15%–20% of infected
personnel. Medical students and staff new to pediatric wards
are at highest risk of acquiring symptomatic RSV infection and
may be least likely to recognize the etiology or significance of
their respiratory illness.
Older adults with underlying conditions. Nosocomial infections from RSV, once thought to be mainly a problem on pediatric wards, are now being recognized on units that house
patients of all ages and are of particular concern for the elderly
and patients with underlying cardiopulmonary and immunosuppressed conditions. Among the institutionalized populations
of older adults, RSV has been shown to be the most commonly
identified viral pathogen associated with respiratory illness, accounting for 27% of such illnesses [10]. Furthermore, in these
groups, RSV-associated illness resulted in significantly greater
morbidity than did infections with other agents, such as
rhinovirus.
Children with underlying conditions. As in the population
at the other end of the age spectrum, in neonates in intensive
care units the recognition and diagnosis of RSV infection is
problematic. Frequently it presents primarily as cardiac or pulmonary decompensation or as a mimic of influenza [11–13].
Similarly, children with underlying cardiopulmonary disease,
especially those with uncorrected congenital heart disease, may
have predominantly cardiac or pulmonary manifestations and
591
are at particularly high risk for subsequent complications
[14–16].
Immunocompromised patients. Of increasing recent interest
and importance is RSV’s potential to become an opportunistic
pathogen in immunocompromised patients [17, 18]. A 3-year
survey of adult cancer patients with respiratory infection at the
M. D. Anderson Cancer Center in Houston identified a respiratory virus in 27%–33% of the illnesses [18]. RSV was the
most frequently isolated agent, accounting for 31% of the infections. About one-half to three-fourths of these infections
were nosocomially acquired. Characteristically a nosocomial
outbreak of RSV on a transplant unit is initiated by RSV being
introduced unrecognized onto the ward by family members or
medical personnel with upper respiratory tract infections, followed by the initially occult spread among the immunocompromised patients.
Circulation of RSV tends to continue for prolonged periods
on these units, even when RSV is no longer present in the
community. In part this may relate to the long duration of
shedding of RSV usually observed with immunocompromised
patients. In these patients, both the amount and length of shedding appear to correlate with the degree of immunosuppression.
In a prospective study of hospitalized immunocompromised
children, those receiving corticosteroid therapy alone had no
worse clinical manifestations of RSV infection than did control
subjects. Shedding, however, was significantly more in quantity
and longer in duration, up to 3 weeks [19]. In those with greater
degrees of immunosuppression, larger quantities of virus were
shed, and the duration of shedding was documented for up to
47 days. Of further concern is the observation that the shedding
in these patients may be detected only intermittently and may
not be associated with the presence of respiratory tract signs
or symptoms. The diagnosis of RSV infection and the initiation
of control measures are frequently delayed for these populations, because the presenting signs accompanying RSV infection are often indistinguishable from those caused by opportunistic pathogens that are more classically associated with the
immunocompromised host. Yet it is important to be constantly
aware of the possibility of RSV infection; the reported mortality
due to RSV infection on transplant units is 20%–100% [18].
Characteristics of RSV that Augment the Chance
of Nosocomial Transmission
RSV’s considerable capability to become a major cause of
nosocomial infection arises from several of its singular characteristics. First, RSV’s epidemiological pattern underscores its
ubiquity and the speed that it spreads: outbreaks of RSV infection
occur every year and spread throughout the country. Second,
persons of all ages, both healthy and with underlying conditions,
are potentially susceptible to RSV infection. In contrast to most
bacterial agents that cause nosocomial illness, nosocomial RSV
infections are not observed primarily in patients with chronic or
592
compromising conditions. Immunity to RSV is incomplete, resulting in repeated infections throughout life, often within short
intervals, even weeks or months [20, 21]. Third, the shedding of
RSV in the respiratory secretions of young children tends to be
for long periods and at high titer. Even adults shed appreciable
quantities of virus for 3 to >7 days [6, 9, 22]. Fourth, RSV in
secretions may remain contagious in the environment for periods
long enough for inadvertent transmission on hands and fomites
[23] (figure 1). Secretions from young children frequently contaminate the objects surrounding their beds, such as crib railings,
table tops, and toys, and may remain viable and contagious for
hours, depending on the type of surface, environmental temperature, and humidity. The usual winter conditions on a ward of
low humidity enhances the duration of RSV’s viability, allowing
it to survive on nonporous surfaces for 6–12 h or more. Furthermore, hand contact with these contaminated surfaces has
been shown to result in transfer of viable, infectious virus to the
skin [23].
Possible Modes of Spread of RSV
Respiratory viruses may be transmitted by any of 3 possible
mechanisms. The first is transmission by small-particle aerosols
(!10 mm mass median diameter), usually generated by coughing
or sneezing, which may traverse distances >1.8 m. Transmission
by small-particle aerosols, therefore, does not require close or
direct contact with the infected subject or with infectious se-
Hall
CID 2000;31 (August)
cretions. Typically, viruses spread by small-particle aerosols
cause explosive outbreaks of infection in a susceptible population, such as occur with measles, varicella, and sometimes
influenza. The second mechanism is transmission by droplets
or large particles. In contrast to aerosols of small particles,
aerosols of large particles require close person-to-person contact, usually at a distance of <0.9 m, for infection to occur.
Third, the virus can also be transmitted via fomites; that is, by
self-inoculation after touching contaminated surfaces. For this
to occur, the virus must be able to remain infectious on environmental surfaces, to be transferred to the skin, and to remain
infectious for a time sufficient to allow self-inoculation into the
respiratory tract.
Studies have indicated that RSV is primarily transmitted by
the latter 2 methods, both of which require close contact with
contagious secretions [24]. In one study, young adult volunteers
working on a pediatric ward were exposed in 3 different manners to infants with RSV infection. The first group, called “cuddlers,” were exposed to an infected infant by caring for the
baby 2–4 h in the usual manner, including feeding, diaper
changing, and playing with the infant. These staff wore gowns
but no mask or gloves. The second group, called “touchers,”
touched with ungloved hand surfaces likely to be contaminated
with the baby’s secretions when the infant was out of the room.
They then gently rubbed the mucous membranes of their nose
or eye, mimicking the manner in which we all unconsciously
rub our eyes or nose. The most effective portals of inoculation
Figure 1. Modes of nosocomial spread of respiratory syncytial virus. Dashed lines, routes of transmission most likely to be interrupted by
infection control; solid lines, routes of transmission unlikely to be affected appreciably by infection control procedures.
CID 2000;31 (August)
Nosocomial RSV Infections
for RSV have been shown experimentally to be the nose and
eyes, in contrast to the mouth, which is a relatively insensitive
site for inoculation [25]. The third group, called “sitters,” was
exposed to an infected baby by sitting at a distance of 11.8 m
from the bed. They wore gowns and gloves, but no masks, and
were allowed to touch only the book they were reading. Cuddlers, therefore, could potentially acquire RSV infection by any
of the 3 routes, whereas touchers could become infected only
by means of fomites and self-inoculation, and sitters only by
small-particle aerosols. Only the cuddlers and touchers became
infected, which suggests that routes that require close or direct
contact with infectious secretions and self-inoculation were the
major or most effective means of transmission. RSV RNA has
been detected by PCR-based methods in air samples from the
rooms of infected patients at distances as far as 7 m from the
patient’s bed and for up to 7 days of hospitalization [26]. This
suggests that small-article aerosol transmission may be possible
but is less efficient than the other routes, considering the lack
of infection in the “sitters” [24]. The RSV detected by polymerase chain reaction in air samples may be largely noninfectious virus.
Controlling the Spread of RSV
How then should we control the spread of nosocomial RSV
infections? First, and probably most importantly, all staff must
understand that they need to be aware of RSV’s capricious
character and covert circulation. Key to any infection control
program is compliance, which will not be forthcoming unless
staff understand that the imposed infection control procedures
are important for their patients’ and their own health. Educational sessions at the beginning of each RSV season are usually helpful. Many studies, however, indicate that compliance
tends to dwindle with time, even over one season, suggesting
the need for educational updates.
Second, surveillance and suspicion of RSV’s presence are
important. Detecting the arrival and disappearance of RSV by
community surveillance will define and limit the time that the
special RSV infection control procedures need to be used. Educational programs should be initiated before the expected RSV
season and the infection control procedures implemented when
RSV is first detected in the community or when the first RSV
admission occurs and the number of infant cases of bronchiolitis and pneumonia begin to rise. For communities that do not
have their own virus surveillance system, the Centers for Disease Control and Prevention (CDC) now monitors RSV activity
around the country on a weekly basis; reports are available on
their Web site (http://www.cdc.gov/). Without this knowledge
of RSV’s activity in the community, determining when RSV
infection control procedures can be discontinued is difficult.
Continuation for ∼2 weeks after the last infant admission for
RSV or when the number of bronchiolitis admissions has returned to baseline may be a reasonable guideline. In units with
593
immunocompromised patients in whom RSV infection has been
documented, precautions should be discontinued only after repeatedly negative cultures spaced over >2 weeks, and vigilance
should be reinstated during periods of enhanced immunosuppression.
The current availability of simple, rapid tests for RSV antigen
has allowed most institutions a means of more specifically diagnosing patients with respiratory illness during the RSV season and may help define the duration of the community outbreak of RSV. These tests also have been beneficial in
determining which patients need to be isolated. However, several caveats should be kept in mind. First, these are generally
screening tests that may miss an appreciable proportion of infections. Their sensitivity and specificity tend to vary according
to the quality of the specimen, the individual product, and the
laboratory, and their positive predictive value markedly declines
when the prevalence of RSV in the community is very low [27].
The third method to control the spread of nosocomial RSV
infections is planning and implementation of control measures
that are both effective and feasible. To have effective measures
that are also feasible is often problematic and necessitates some
degree of variability among individual institutions. The CDC
advises the use of contact precautions, in addition to standard
precautions, for RSV infections (table 1) [28]. Contact precautions are recommended for microorganisms that can be spread
by direct patient contact (as occurs during care procedures that
involve touching the dry skin of the patient) or by indirect
contact, that is, touching surfaces or items in the patient’s environment that may be contaminated [28]. They class the evidence for these recommendations as “category I-B,” which is
based “on strong rationale and suggestive evidence” and is
strongly recommended and “reviewed as effective by experts in
the field” [28]. Included are recommendations to wash hands,
to wear gloves, masks, eye protection, and gowns, and to house
patients infected with RSV in private rooms or in a cohort
isolated from other patients (table 1). Studies evaluating the
smorgasbord of possible infection control procedures are confusing and often conflicting [28]. The differing reported efficacy
and permutations of procedures available make it difficult, if
not impossible, to conclude that a single combination of procedures is most effective and evidence-based. The possible exception to this is hand washing.
Hand washing. Most experts concur that hand washing is
central to any infection control program, and the CDC also
labels hand washing as category I-B [28]. However, no methods
have been developed to ensure continued compliance with hand
washing or to monitor how effectively and assiduously hospital
staff wash their hands. Important in promoting frequent and
effective hand washing are the convenience and number of
sinks, the acceptability of the soap or cleansing agent and towels, and their accessibility. For these reasons, the newer alcoholbased hand rub agents, which do not require a sink and water,
may be useful [29]. Although studies have not examined the
594
Hall
CID 2000;31 (August)
Table 1. Infection control procedures, both standard precautions and contact precautions, for prevention of
respiratory syncytial virus (RSV) infection.
Recommendation category, procedure
Comment(s)
a
Category I-B recommendations
Hand washing
b
Wearing gloves
b
Wearing gowns
b
Wearing masks plus eye protection
Housing patients in private rooms or in a cohort isolated
b
from other patients
Use of dedicated patient-care equipment
Sometimes recommended with less or no supporting evidence
Staff assigned according to patient’s RSV status
b
Visitor restrictions during RSV season
Screening visitors for illness during RSV season
Water with soap or antibacterial agent or waterless antiseptic
hand rub
Combined with hand washing before and after each glove
change; may diminish self-inoculation
When direct contact with patient or patient secretions is likely
Eyes and nose are major sites for inoculation
Patients with documented infection can be grouped and isolated
from other patients; beds should be separated by 10.9 m
Equipment, including toys, assigned to specific patients
Specific staff care only for patients with RSV infection
Some qualify by restricting young children only
Visitors assessed by trained personnel and/or advised by use of
an educational patient information sheet
a
Centers for Disease Control and Prevention recommendations based “on strong rationale and suggestive evidence” and strongly
recommended and “reviewed as effective by experts in the field” [28].
b
See text for further qualifications and alternatives.
comparative efficacy of these products for RSV, experiments in
our laboratory have shown RSV to be a labile virus that is
quickly rendered noninfectious by a variety of agents, including
alcohol and mild soaps with water [23].
Gloves. The use of gloves along with gowns has been shown
to reduce the rate of nosocomial RSV infections [30]. However,
gloves should be changed and the hands washed between tasks
involving the same patient, as well as between patients [28].
Bacterial contamination on the hands of gloved personnel has
been demonstrated [29, 31], and RSV survives on gloves for
longer than on the skin of the hands [23]. Nevertheless, gloves
may be effective in the control of RSV because few persons
will pick their noses or rub their eyes while gloved, and therefore
the chance for self-inoculation is diminished.
Gowns. The use of gowns is advisable if the staff member
is to have direct contact with the infected patient such that contamination of clothing with patient secretions is likely, on the
basis of evidence that RSV in secretions on clothing may remain
infectious for 1 h [23]. The expense associated with gown use
can be considerable; it can be diminished by not requiring the
use of gowns by all persons entering the room but only by those
who have intimate contact with the patient, and also sometimes
by allowing the reuse of a gown kept by the patient’s bedside.
Of note, but unexplained, is the finding that no particular isolation policy in a multivariate model was associated with a decreased rate of RSV nosocomial infections in 9 Canadian pediatric hospitals, but gowning to enter the room was actually
associated with an increased risk of RSV transmission [5].
Masks. It has not been clearly shown that wearing masks
has any additional benefit. Most studies use of masks do so as
part of multiple infection control procedures, not allowing delineation of any additional possible benefit from masks alone.
However, masks without eye protection may offer only limited
protection, given that the eyes are also effective portals of inoculation for RSV. Therefore masks, if appropriately used, may
act as a barrier for 1 of the 2 most effective sites for inoculation
of RSV. The use of eye-nose goggles has been shown to be
beneficial [32]. Their use, however, may be limited by acceptability and additional expense, and much of their benefit could
probably be achieved by strict hand washing.
Isolation of patients. If feasible, patients with acute respiratory illness should be isolated during the RSV and influenza
seasons until the etiology of the illness is determined. The use
of rapid detection assays has been helpful in determining which
patients may be housed together. However, during the busy
RSV season, when pediatric wards tend to be overcrowded,
there may not be enough single bedrooms available. Several
observations suggest that isolation may not be essential. First,
RSV is primarily spread by close or direct contact; that is, largeparticle aerosols and fomites. Because large-particle aerosols
traverse distances of only 0.9 m, spacing beds by 10.9 m should
prevent transmission by this route from patient to patient. Fomite-mediated transmission is probably controlled more effectively by strict hand washing and by education of staff and
family members than by separating patients. A study by Wenzel
et al. [33] questions whether single bedrooms are required for
children with respiratory virus infections. They demonstrated
that for a patient in a multibed room, the risk of becoming
infected with a virus shed by a roommate was only 3%. Thus,
when single-bed rooms are limited, it may be best to reserve
them for patients with underlying conditions that put them at
high risk for severe or complicated RSV infection.
Assignment of personnel and equipment to specific patients.
Assigning staff to care only for patients with or without RSV
infection theoretically should limit the chance of staff acting as
vectors of transmission of RSV from an infected to an uninfected patient by contamination of their hands from fomites.
This policy, however, is unlikely to be feasible, and any additional benefit it may offer could be equaled by emphasizing
strict hand washing. Transmission of RSV by infected person-
CID 2000;31 (August)
Nosocomial RSV Infections
nel, even those with mild respiratory symptoms, however, is of
concern. Ward personnel manifesting any respiratory symptoms should be reminded about the need for hand washing and
good infection control procedures and, if possible, should avoid
caring for high-risk patients. Equipment for patient care, including toys, should be assigned to use by individual patients.
All reusable equipment should not be used for another patient
until it is properly cleaned, even if the other patient is also
infected and staying in the same room.
Visitor restrictions. Family and other visitors during the
RSV season frequently are infected with RSV and may transmit
it to uninfected patients. Studies analyzing the antigenic and
genomic diversity among isolates of RSV obtained during nosocomial outbreaks have shown that multiple strains tend to
circulate during a single outbreak [34, 35]. A number of policies
have been devised to guard against this possibility of visitors
introducing RSV onto a ward. Some prohibit all young children
from visiting during the RSV season. The relative benefit of
this prohibition must be considered in each institution. In addition, such a policy does not recognize the frequent RSV infections that occur in older children and adults. One-third or
more of the adult family members of a child infected with RSV
may acquire the infection, and ∼15% of these infections are
asymptomatic. Screening of visitors for acute respiratory symptoms, if feasible, may prevent some possible infections being
transmitted, but many factors, such as the duration of symptoms and the accuracy and quality of the screening, make the
effectiveness of this procedure variable. A reasonable policy,
nevertheless, is to educate family members at the time of the
patient’s admission about the risks visiting when ill and the
importance of limiting their visit, especially if they bring young
children. Precautions against introduction of infection by visitors, however, must be much more stringent on transplant units
and other wards that house high-risk patients for whom the
potential benefit of avoiding devastating nosocomial infection
outweighs the extra educational and monitoring efforts of the
staff.
Other means of controlling RSV in the hospital. There is
currently no vaccine or generally feasible and effective means
of prevention of RSV infection in or out of the hospital setting.
The first means of prophylaxis for some high-risk infants only
became available in 1996, when high-titer polyclonal immunoglobulin to RSV (RespiGam; MedImmune, Gaithersburg,
MD) was licensed. This is approved only for high-risk premature infants and requires monthly iv administration [36]. The
subsequent licensing of a humanized monoclonal antibody, palivizumab (Synagis; MedImmune), has offered the advantages
of monthly im administration, which has fewer adverse effects
and can be used for outpatients [36]. This product was produced
from a mouse monoclonal antibody that recognizes a protective
epitope of the immunologically important surface glycoprotein,
the F protein. However, these products are approved for prophylaxis only for the small group of premature infants who are
595
!36 weeks’ gestational age and/or have chronic lung disease
and still require medical therapy. The pivotal multicenter trial
that led to approval for monthly prophylaxis for these highrisk infants was a placebo-controlled trial of 1502 premature
infants, which demonstrated that the rate of subsequent hospitalization for RSV illness was 10.6% in the placebo group
and 4.8% in the infants receiving prophylaxis, which was a 55%
reduction in the rate of hospitalization [37]. The product is not
approved for use in other groups, and the American Academy
of Pediatrics advises against using it to prevent nosocomial RSV
infection, preferring other traditional infection control procedures [36]. Furthermore, the effectiveness of this product as
prophylaxis in other groups of patients or in other settings has
not been adequately evaluated, and the significant expense, even
for small infants, prohibits widespread use.
Polyclonal RSV immunoglobulin has been evaluated in a
relatively small group of infants as therapy and has not been
shown to be of clear benefit. High-titer polyclonal immunoglobulin to RSV with or without ribavirin has also been suggested as prophylaxis for hospitalized patients beyond infancy
who are at high risk for severe or complicated RSV infection,
especially transplant recipients [19, 38]. No controlled studies,
however, are yet available to support this use.
Summary
Although 60 years have elapsed since the Adams’ [1] initial
description of a nosocomial outbreak of pneumonia among
infants due to a virus that was subsequently identified as RSV,
no truly effective means exists to control the capricious circulation of RSV in the hospital environment. The difficulty in
evaluating and quantitating the benefit of any one or multiple
infection control procedures does not allow recommendation
of a single set of procedures from the array of available interventions. Based on many years of studies, we know that each
has potential advantages and disadvantages and that each institution must judge which procedures are best to use based on
their relative benefit, cost, feasibility, and acceptability.
Nevertheless, an infection control policy to curb the spread
of RSV is advisable, indeed essential, if we are to diminish the
appreciable morbidity and mortality now recognized to be associated with nosocomial RSV infection in high-risk patients.
Of prime importance is that each institution be prepared. Whatever prevention program an institution adopts, it needs to be
fully developed and ready for implementation as soon as surveillance data indicate RSV’s annual arrival in the community.
Central to any such program is the education and reeducation
of all staff about the characteristics, transmission, and risk of
nosocomial RSV infection for patients and for themselves, because compliance depends on it. The choice of which infection
control procedures to use is best based on understanding the
mechanisms by which RSV spreads. Good hand washing is
probably the single most important procedure.
596
Hall
CID 2000;31 (August)
References
1. Adams J. Primary virus pneumonitis with cytoplasmic inclusion bodies; a
study of an epidemic involving thirty-two infants with nine deaths. JAMA
1941; 116:925–33.
2. Adams J, Imagawa D, Zike K. Epidemic bronchiolitis and pneumonia related
to respiratory syncytial virus. JAMA 1961; 176:1037–9.
3. Hall C, Douglas RJ, Geiman J, et al. Nosocomial respiratory syncytial virus
infections. N Engl J Med 1975; 293:1343–6.
4. Hall C. The nosocomial spread of respiratory syncytial virus infections. Annu
Rev Med 1983; 34:311–9.
5. Langley J, LeBlanc J, Wang E, et al. Nosocomial respiratory syncytial virus
infection in Canadian pediatric hospitals: a pediatric investigators collaborative network on infections in Canada study. Pediatrics 1997; 100:943–6.
6. Hall C, Kopelman A, Douglas RJ. Neonatal respiratory syncytial viral infections. N Engl J Med 1979; 300:393–6.
7. Forster J, Schumacher R. The clinical picture presented by premature neonates infected with the respiratory syncytial virus. Eur J Pediatr 1995;
154:901–5.
8. Gouyon J, Pothier P, Guignier F, et al. Outbreak of respiratory syncytial
virus in France. Eur J Clin Microbiol 1985; 4:415–6.
9. Hall C, Geiman J, Douglas RJ, et al. Control of nosocomial respiratory
syncytial viral infections. Pediatrics 1978; 62:728–31.
10. Falsey AR, Treanor JJ, Betts RF, Walsh EE. Viral respiratory infections in
the institutionalized elderly: clinical and epidemiologic findings. J Am
Geriatr Soc 1992; 40:115–9.
11. Falsey AR, Cunningham CK, Barker WH, et al. Respiratory syncytial virus
and influenza A infections in the hospitalized elderly. J Infect Dis 1995;
172:389–94.
12. Guidry GG, Black-Payne CA, Payne DK, Jamison RM, George RB, Bocchini JA Jr. Respiratory syncytial virus infection among intubated adults
in a university medical intensive care unit. Chest 1991; 100:1377–84.
13. Walsh E, Falsey A, Hennessey P. Respiratory syncytial virus and other virus
infections in persons with chronic cardiopulmonary disease. Am J Respir
Crit Care Med 1999; 160:791–5.
14. MacDonald N, Wolfish N, McLaine P, et al. Role of respiratory viruses in
exacerbations of primary nephrotic syndrome. J Pediatr 1986; 108:378–82.
15. Isaacs D, Dickson H, O’Callaghan C, et al. Handwashing and cohorting in
prevention of hospital acquired infections with respiratory syncytial virus.
Arch Dis Child 1991; 66:227–31.
16. Mahant S, Robinson F, Wang E. Hospital morbidity in patients with RSV
lower respiratory illness (LRI) and underlying heart disease: analysis of
PICNIC RSV database. Pediatr Res 1997; 41:78A.
17. Harrington RD, Hooton TM, Hackman RC, et al. An outbreak of respiratory
syncytial virus in a bone marrow transplant center. J Infect Dis 1992; 165:
987–93.
18. Couch R, Englund J, Whimbey E. Respiratory viral infections in immunocompetent and immunocompromised persons. Am J Med 1997; 102:2–9.
19. Hall CB, Powell KR, MacDonald NE, et al. Respiratory syncytial viral
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
infection in children with compromised immune function. N Engl J Med
1986; 315:77–80.
Hall C, Walsh E, Long C, et al. Immunity to and frequency of reinfection
with respiratory syncytial virus. J Infect Dis 1991; 163:693–8.
Henderson F, Collier A, Clyde WJ, et al. Respiratory syncytial virus infections, reinfections and immunity. N Engl J Med 1979; 300:530–4.
Hall C, Douglas RJ, Geiman J. Respiratory syncytial virus infections in
infants: quantitation and duration of shedding. J Pediatr 1976; 89:11–5.
Hall C, Geiman J, Douglas RJ. Possible transmission by fomites of respiratory syncytial virus. J Infect Dis 1980; 141:98–102.
Hall C, Douglas RJ. Modes of transmission of respiratory syncytial virus. J
Pediatr 1981; 99:100–3.
Hall C, Douglas RJ, Schnabel K, et al. Infectivity of respiratory syncytial
virus by various routes of inoculation. Infect Immun 1981; 33:779–83.
Aintablian N, Walpita P, Sawyer M. Detection of Bordetella pertussis and
respiratory syncytial virus in air samples from hospital rooms. Infect Control Hosp Epidemiol 1998; 19:918–23.
Kellogg JA. Culture vs. direct antigen assays for detection of microbial pathogens from lower respiratory tract specimens suspected of containing respiratory syncytial virus. Arch Pathol Lab Med 1991; 451–8.
Garner JS. Guidelines for isolation precautions in hospitals. Infect Control
Hosp Epidemiol 1996; 17:53–80.
Larson EL. APIC guideline for hand washing and hand antisepsis in health
care settings. Am J Infect Control 1995; 23:251–69.
Leclair J, Freeman J, Sullivan B, et al. Prevention of nosocomial respiratory
syncytial virus infections through compliance with glove and gown isolation precautions. N Engl J Med 1987; 317:329–34.
Olsen RJ, Lynch P, Coyle MB, Cummings J, Bokete T, Stamm WE. Examination gloves as barriers to hand contamination in clinical practice.
JAMA 1993; 270:350–3.
Gala C, Hall C, Schnabel K, et al. The use of eye-nose goggles to control
nosocomial respiratory syncytial virus infection. JAMA 1986; 256:2706–8.
Wenzel R, Deal E, Hendley J. Hospital-acquired viral respiratory illness on
a pediatric ward. Pediatrics 1977; 60:367–371.
Storch GA, Hall CB, Anderson LJ, Park CS, Dohner DE. Antigenic and
nucleic acid analysis of nosocomial isolates of respiratory syncytial virus.
J Infect Dis 1993; 167:562–6.
Mazzulli T, Peret T, McGeer A, et al. Molecular characterization of a nosocomial outbreak of human respiratory syncytial virus on an adult leukemia/lymphoma ward. J Infect Dis 1999; 180:1686–9.
American Academy of Pediatrics, Committee of Infectious Diseases. Prevention of respiratory syncytial virus infections: indications for use of
palivizumab and update on the use of RSV-IVIG. Pediatrics 1998; 102:
1211–6.
IMpact-RSV Study Group. Palivizumab, a humanized respiratory syncytial
virus monoclonal antibody, reduces hospitalization from respiratory syncytial virus infection in high-risk infants. Pediatrics 1998; 102:531–7.
Whimbey E, Englund JA, Couch RB. Community respiratory virus infections
in immunocompromised patients with cancer. Am J Med 1997; 102:10–8.